Inflammation (irritation with swelling and presence of increased numbers of immune cells) caused by immune responses to toxins, medications, infection, or other disorders may injure the structures of the kidney, leading to various types of glomerulonephritis or acute tubular necrosis (tissue death). Autoimmune disorders may also damage the kidneys. Injury to the kidney may result in short-term damage with minimal or no symptoms, or it can be life-threatening as in the case of acute renal failure or chronic renal failure.
Most forms of chronic kidney disease (CKD) progress inexorably to end stage renal disease (ESRD), which has considerable morbidity and a 20% annual mortality. While the initiators of CKD vary, it is generally accepted that secondary processes common to all renal diseases ensue, establishing a vicious cycle of progressive nephron destruction leading to glomerulosclerosis and tubulo-interstitial fibrosis. A growing body of evidence suggests that renal inflammation is a key secondary process driving progression of such disorders.
Immunosuppressants including glucocorticoids, which directly inhibit NF-kB activity are widely used to treat patients with excessive acute or chronic renal inflammation. However, these drugs often prove to be marginally effective and have been associated with significant adverse side effects. There is an urgent need for effective treatments of kidney inflammation and disease with fewer adverse side effects.